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Sökning: swepub > Umeå universitet > (2000-2004)

  • Resultat 6661-6670 av 7059
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6661.
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6662.
  • Waterworth, Eva Lindh, et al. (författare)
  • Mood Devices : Interactive media and mental health
  • 2004
  • Ingår i: E-Society 2004 : proceedings of the IADIS International Conference, Ávila, Spain, July 16-19, 2004. - : IADIS Press.
  • Konferensbidrag (refereegranskat)abstract
    • We introduce Mood Devices, interactive digital media and environments designed to alter the inter-actor’s psychological state. In particular, we describe three very different virtual reality (VR) environments: Relaxation Island, the Exploratorium, and the Achievement Room, developed with our partners as part of the EMMA (Engaging Media for Mental Health) project. Relaxation Island is designed to support established relaxation techniques, as part of interventions to assist individuals cope with specific anxieties such as examination stress. The Achievement Room gives users with chronic restricted mobility the opportunity to sing and play in a virtual concert, in front of an audience of avatars programmed to respond to their performance. The aim is to provide a sense of achievement and encourage a more positive attitude. The Exploratorium, as the name suggests, takes a more user-directed approach: It provides an environment that can be explored in an embodied way, with three specific zones designed to elicited widely different moods. All three environments can be run on a range of platforms, from high-end immersive VR, to pocket-sized PDAs and web-based applications. We see such interactive media as providing an important contribution to the future of ehealth programmes.
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6663.
  • Waterworth, John, et al. (författare)
  • Relaxation Island : A Virtual Tropical Paradise. Interactive Experience
  • 2004
  • Ingår i: Proceedings of BCS HCI2004: Designing for Life, Leeds, UK, September 2004..
  • Konferensbidrag (refereegranskat)abstract
    • We present Relaxation Island, one of several Mood Devices we have developed with our partners as part of the EMMA (Engaging Media for Mental Health Applications) project. Mood Devices are interactive digital media and environments designed to alter the inter-actor’s psychological state. Relaxation Island was designed to support established relaxation techniques, as part of interventions to assist individuals cope with specific anxieties such as examination stress, and also simply as a virtual place where anyone can go to relax. Attendees of this interactive experience will have the opportunity to relax on the island, navigating around the virtual space using a novel wireless “seashell” device
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6664.
  • Waterworth, John, et al. (författare)
  • The Reality Helmet : Transforming the Experience of Being-in-the-World
  • 2003
  • Ingår i: Proceedings of HCI 2003: Designing for Society (Bath, UK, September 8-12). - Bath, UK : British HCI Group. ; , s. 1-4
  • Konferensbidrag (refereegranskat)abstract
    • The Reality Helmet is a wearable device providing a novel form of interactive experience, in which the user’s vision and hearing is completely shielded off from the world. Video and sounds are sampled by the Helmet from the surrounding environment, but through computer processing sounds are presented to the wearer as vision and sights are turned into a soundscape. The result is a radical transformation of the nature of being in the world, an extreme form of artificial synaesthesia. The Reality Helmet leads its wearer to question the relationship between what is out there and what is sensed. Conference participants will be invited to wear the Helmet and experience a different way of being in the world.
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6665.
  • Weber, M., et al. (författare)
  • Preserved slow conducting corticomotoneuronal projections in ALS patients with autosomal recessive D90A CuZn-SOD mutation.
  • 2000
  • Ingår i: Brain. - : Oxford University Press (OUP). - 0006-8950 .- 1460-2156. ; 123:7, s. 1505-1515
  • Tidskriftsartikel (refereegranskat)abstract
    • Recently, a subgroup of the amyotrophic lateral sclerosis (ALS) syndrome associated with mutations in the gene encoding the free radical scavenging enzyme CuZn-superoxide dismutase (CuZn-SOD, SOD1) has been identified. Some 67 different mutations have been reported worldwide to date, comprising about one-fifth of familial ALS cases in the populations studied. The autosomal recessively inherited D90A CuZn-SOD mutation has been associated with a very slowly progressive, clinically distinct phenotype, and is neurophysiologically characterized by very slow central motor conduction. It is not known which physiological and/or biochemical mechanisms are responsible for the different clinical course. To delineate ALS associated with this particular CuZn-SOD mutation from ALS without mutations, we performed a detailed neurophysiological study of the corticomotoneuronal function using peristimulus time histograms (PSTHs) in eight ALS patients homozygous for the D90A CuZn-SOD mutation. The results were compared with those obtained in 12 non-hereditary ALS patients and 11 healthy subjects. PSTHs were constructed from three to seven different, voluntarily recruited motor units of the extensor digitorum communis muscle (EDC) in each patient. The onset latency, number of excess bins, duration and synchrony of the primary peak were analysed. All measurements differed significantly between healthy controls and the D90A patients (P < 0.0007). The mean onset latency of the primary peak in D90A patients was 35.3 ms, compared with 24.2 ms for non-hereditary ALS patients and 19.3 ms for normal subjects (P < 0.0000). Delayed primary peaks in the D90A patients were desynchronized and characteristically preceded by a marked suppression phase. This suppression phase was not seen in non-hereditary ALS patients. We conclude that the mainly slow conducting and/or polysynaptic corticomotoneuronal connections are preserved in the D90A homozygous cases, and that the cortical and possibly spinal inhibitory circuitry is preserved. These events may partially protect the motor neurons, slowing down the degenerative process.
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6666.
  • Weber, M., et al. (författare)
  • The physiological basis of conduction slowing in ALS patients homozygous for the autosomal recessive D90A CuZn-SOD mutation
  • 2001
  • Ingår i: Muscle and Nerve. - 0148-639X .- 1097-4598. ; 24:1, s. 89-97
  • Tidskriftsartikel (refereegranskat)abstract
    • Familial amyotrophic lateral sclerosis (ALS) with the autosomal-recessively inherited D90A CuZn-superoxide dismutase (CuZn-SOD) mutation is characterized by a stereotypic slowly progressive, distinctive phenotype and very slow central motor conduction. To determine the basis of this slowing, we assessed corticomotoneuronal function using peristimulus time histograms (PSTHs) in 8 ALS patients homozygous for the D90A CuZn-SOD mutation. The results were compared with findings in 10 patients with multiple sclerosis (MS), in which slowing of central motor conduction is common, and 11 healthy subjects. PSTHs were constructed from 3-7 different, voluntarily recruited motor units recorded in each patient from the extensor digitorum communis muscle (EDC). In D90A and MS patients, the stimulus threshold, onset latency, number of excess bins, duration, amplitude, and synchrony of the primary peak differed significantly from controls (P < 0.0004). The mean onset latency of the primary peak in D90A patients was 35.3 ms, compared to 23.6 ms for MS patients and 19.3 ms for normal subjects (P < 0.0001). In the D90A patients, the onset latencies of the primary peak had a bimodal distribution, whereas in MS the distribution showed a continuum. Loss of synchrony was similar in D90A and MS patients, but the threshold, number of excess bins, and duration differed significantly (P < 0.0057), which suggests that either axonal loss or demyelination can result in delayed and desynchronized primary peaks. We propose that conduction slowing in the D90A homozygotes results from selective loss of fast-conducting large pyramidal cells with preservation of slow-conducting mono- or polysynaptic corticomotoneuronal connections. Copyright 2001 John Wiley & Sons, Inc.
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